Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyruvate plays a central role in intermediary metabolism. Pyruvate, however, is also a potent antioxidant and free radical scavenger, and numerous studies have shown that treatment with this compound can be salutary in numerous pathologic conditions that are thought to be mediated, at least in part, by redox-dependent phenomena. Unfortunately, aqueous solutions of pyruvate rapidly undergo an aldol-like condensation reaction to form 2-hydroxy-2-methyl-4-ketoglutarate (parapyruvate), a compound that is a potent inhibitor of a critical step in the mitochondrial tricarboxylic acid cycle. To circumvent this issue, our laboratory formulated a derivative of pyruvic acid, ethyl pyruvate, in a calcium- and potassium-containing balanced salt solution. We showed that treatment with this fluid could ameliorate much of the structural and functional damage to the intestinal mucosa caused by mesenteric ischemia and reperfusion in rats. In subsequent studies, we showed that treatment with ethyl pyruvate solution could improve survival in rodent models of hemorrhagic shock and resuscitation and also down-regulate a number of proinflammatory genes. Recently, ethyl pyruvate was also shown to improve survival in murine models of acute endotoxemia and bacterial peritonitis. Although the biochemical basis for the anti-inflammatory actions of pyruvate remain to be elucidated, this simple compound warrants further evaluation as a treatment for a number of conditions commonly encountered in the practice of critical care medicine.
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PMID:Ethyl pyruvate: a novel anti-inflammatory agent. 1254 77

Electrolyte and acid-base disturbances are frequent in patients with end-stage liver disease; the underlying physiopathological mechanisms are often complex and represent a diagnostic and therapeutic challenge to the physician. Usually, these disorders do not develop in compensated cirrhotic patients, but with the onset of the classic complications of cirrhosis such as ascites, renal failure, spontaneous bacterial peritonitis and variceal bleeding, multiple electrolyte, and acid-base disturbances emerge. Hyponatremia parallels ascites formation and is a well-known trigger of hepatic encephalopathy; its management in this particular population poses a risky challenge due to the high susceptibility of cirrhotic patients to osmotic demyelination. Hypokalemia is common in the setting of cirrhosis: multiple potassium wasting mechanisms both inherent to the disease and resulting from its management make these patients particularly susceptible to potassium depletion even in the setting of normokalemia. Acid-base disturbances range from classical respiratory alkalosis to high anion gap metabolic acidosis, almost comprising the full acid-base spectrum. Because most electrolyte and acid-base disturbances are managed in terms of their underlying trigger factors, a systematic physiopathological approach to their diagnosis and treatment is required.
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PMID:Electrolyte and Acid-Base Disturbances in End-Stage Liver Disease: A Physiopathological Approach. 2850 71